Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.37 (neutrophil elastase)
 4,078 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to the literature, Cyclosporine A (CsA) is said to suppress specifically the activity of T and B cells. A significant influence on phagocyte function has been neglected. However, aggravated courses of bacterial and fungal infections have been frequently reported under the treatment with CsA, suggesting that a latent depression of phagocytic activity may possibly occur under clinical circumstances. Therefore, this study set out to assess whether CsA can also change granulocyte function under therapy conditions or not. Thirty-seven patients, 3 months-10 years after kidney transplantation being under immunosuppressive treatment with CsA + Prednisolone (n = 25), Azathioprine + Prednisolone (n = 6) and under Prednisolone alone (n = 6) underwent the study. 18 healthy persons served as a normal control group. Granulocyte function was tested ex vivo by chemiluminescence (CL) after stimulation with phorbolmyristate acetate (PMA) and with zymosan (zym) activated autologous or pool-serum. The obtained data were correlated to corresponding serum or plasma levels of CsA, human leukocyte elastase (HLE) and neopterin. Comparing the three therapy groups with the healthy control and with each other no differences could be seen in median CL values; but there was a significant (p = 0.05) negative correlation between CsA blood levels and maximum CL values of PMN. Such inhibition of CL could be calculated for zym but not for PMA stimulated PMN; suggesting that the CsA mediated inhibition of granulocyte function may be only partial and restricted to phagocytosis. In addition, a positive correlation between serum levels of human leukocyte elastase (HLE) and neopterin could be found. This indicates a simultaneous influence of CsA on both PMN and macrophages.
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PMID:Latent inhibition of granulocyte function by cyclosporine A. 227 42

A novel colitis model using Syrian hamsters was developed. Colitis was induced by intracolonic administration of 1% acetic acid, and the ulcer area, tissue myeloperoxidase (MPO) activity, and luminal neutrophil elastase (NE) activity of the colon were determined at 1, 3, 8, 24 and 48 hr after colitis induction. The histopathological changes of the colon were also examined in this model. An increase of tissue MPO activity and NE activity was evident at 3 hr after induction of colitis, peaked at 24 hr, and decreased subsequently. The increase of luminal NE activity was well correlated with the colonic ulcer area. In histopathological examination, ulceration, erosion, crypt abscesses, neutrophil infiltration, hemorrhage, and edema were seen. The effects of prednisolone were examined to evaluate the adequacy of our colitis model. Syrian hamsters were treated orally with prednisolone at 18 and 1 hr before and at 6 hr after induction of colitis, and the ulcer area, tissue MPO activity, and luminal NE activity were evaluated at 24 hr after colitis induction. Prednisolone therapy had little effect on the tissue MPO activity. However, the NE activity of the prednisolone-treated group was significantly decreased. In addition, although prednisolone did not significantly decrease the ulcer area, a tendency toward decrease was noted. We conclude that this new model of experimental colitis in Syrian hamsters is useful for investigating the pathophysiology of colitis, especially useful for studying the relationship between colitis and NE activity.
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PMID:Colonic ulceration and increase of neutrophil elastase activity in the acetic acid-induced colitis model in Syrian hamsters. 1513 72

We developed a colitis model in Syrian hamsters (Mesocricetus auratus) to investigate the relationship between colitis and neutrophil elastase (NE). Colitis was induced by a single intracolonic dose of trinitrobenzene sulfonic acid (TNBS; 90 mg/ml) dissolved in 15% (vol/vol) ethanol. The ulcer area, tissue myeloperoxidase (MPO) activity, and luminal NE activity all were increased on Days 1 and 5, corresponding with the acute inflammatory histopathological changes. These acute inflammatory parameters subsequently decreased by Day 14, and chronic inflammatory histopathological changes became evident. Recurrence of inflammation was not observed during the period up to Day 28. To evaluate our colitis model, the effects of prednisolone were examined. Prednisolone was administered orally once on the day before induction of colitis, and animals were treated twice daily thereafter. Although prednisolone had little effect on the tissue MPO activity, prednisolone inhibited the ulcer area and NE activity. In addition, the effects of an NE-specific inhibitor (ONO-6818) on our TNBS-induced colitis model were examined. In the subcutaneous treatment study, ONO-6818 was administered once before the induction of colitis. Although ONO-6818 had little effect on the tissue MPO activity, the ulcer area and NE activity were decreased in the ONO-6818-treated group. The inhibitory effects on the ulcer area and NE activity were confirmed after oral treatment with ONO-6818 after induction of colitis. We conclude that our colitis model is useful for investigating the relationship between colitis and NE, and inhibition of NE activity can prevent the progression of ulceration.
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PMID:Pathophysiological studies of trinitrobenzene sulfonic acid-induced colitis in Syrian hamsters (Mesocricetus auratus). 1576 9